Cardiac Surgery-Associated Acute Kidney Injury in Adults: Clinical Outcomes, Prevention Strategies, and Future Therapies in the Postoperative Period.

Cardiac surgery-associated acute kidney injury (CSA-AKI) is a major postoperative complication that results in significant morbidity and mortality. Causes are heterogeneous, treatment strategies are largely supportive, and data on outcomes, such as potential for recovery, are lacking. This literature review explores the evidence on how furosemide may alter the course and outcome of postoperative fluid overload in patients with CSA-AKI.

A Multivariate Analysis of Pain and Distress in Adults Undergoing BMAB.

Clinicians routinely perform bone marrow aspiration and biopsy (BMAB) to diagnose cancer and evaluate disease status; however, few studies address pain and distress with BMAB. A prospective descriptive-correlational design examined patients' ( = 152) ratings of pain intensity (numeric rating scale, 0-10) and distress (distress thermometer) at baseline and 5 min and 1 hr postprocedure. Data were analyzed using descriptive statistics, chi-square, and linear regression models.

Colon tumour cells increase PGE(2) by regulating COX-2 and 15-PGDH to promote survival during the microenvironmental stress of glucose deprivation.

Due to poor tumour-associated vasculature, tumour cells are subjected to a fluctuating microenvironment with periods of limited oxygen and glucose availability. Adaptive mechanisms to adverse microenvironments are important for tumour cell survival. The cyclooxygenase (COX)-2/prostaglandin E(2) (PGE(2)) pathway has key roles in colorectal tumorigenesis.

HGF/Met signalling promotes PGE(2) biogenesis via regulation of COX-2 and 15-PGDH expression in colorectal cancer cells.

Evidence points towards a pivotal role for cyclooxygenase (COX)-2 in promoting colorectal tumorigenesis through increasing prostaglandin E(2) (PGE(2)) levels. PGE(2) signalling is closely associated with the survival, proliferation and invasion of colorectal cancer cells. Recently, a reduction in PGE(2) inactivation, a process mediated by the nicotinamide adenine dinucleotide (NAD+)-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH), has also been shown to promote tumoral PGE(2) accumulation.

The COX-2/PGE2 pathway: key roles in the hallmarks of cancer and adaptation to the tumour microenvironment.

It is widely accepted that alterations to cyclooxygenase-2 (COX-2) expression and the abundance of its enzymatic product prostaglandin E(2) (PGE(2)) have key roles in influencing the development of colorectal cancer. Deregulation of the COX-2/PGE(2) pathway appears to affect colorectal tumorigenesis via a number of distinct mechanisms: promoting tumour maintenance and progression, encouraging metastatic spread, and perhaps even participating in tumour initiation. Here, we review the role of COX-2/PGE(2) signalling in colorectal tumorigenesis and highlight its ability to influence the hallmarks of cancer--attributes defined by Hanahan and Weinberg as being requisite for tumorigenesis.